In further studies of experimental allergic encephalomyelitis (EAE), special attention will be focused on: (1) the role of the clotting cascade and perivascular deposits of fibrin and edema within the peripheral and central nervous system as important determinants of clinical neurologic signs of EAE in rats, (2) the participation of circulating antibody, including immunoglobulin-E, in pathogenesis of clinical signs of EAE in rats, (3) the nature of EAE-transfer activity demonstrable in cell-free supernatants of incubated rats' sensitized lymphoid cells, (4) further definition of the EAE-adjuvanticity of synthetic polyribonucleotides in guinea pigs, (5) dissection of the mechanisms underlying the potentiation of EAE by total body irradiation and persistence of measles virus in nervous tissue of hamsters.